电子垃圾重金属暴露人群MNed BNC及其影响因素的研究
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摘要
铅、镉、铜、镍等重金属已广泛用于各种电子产品。大量淘汰的电子产品带来了新的环境问题。由于众多简易作坊以原始简陋的方法手工拆解电子垃圾,导致其中的有害物质如多溴联苯醚(Polybrominated Diphenyl Ethers, PBDEs)、多环芳烃(Polycyclic Aromatic Hydrocarbons, PAHs)和重金属进入大气,水体和土壤等环境介质,对健康构成潜在的威胁。已知铅、镉、铜、镍等重金属可经多途径侵入机体,损害机体的多个系统。例如,铅是以神经毒性为主的一种重金属元素且毒性很强,它可累及全身各系统,如造血系统、消化系统、心血管系统以及免疫系统。已知镉是确认的致癌物。当机体长期暴露镉后,不仅其肾脏功能受影响,而且其两性生殖系统功能也可受损。镍污染能引起人类呼吸系统的癌症。铜虽是人体的必需微量元素,但是机体过量暴露铜后,则可导致机体正常代谢失衡。
近年,电子垃圾产生的环境问题已引起社会的广泛关注。但是有关电子垃圾污染物暴露人群可能的生物学效应研究的报导却十分有限。本研究选择我国南方某电子垃圾拆解地居民58名为暴露组,地理环境和生活习惯相近且无明显已知污染源存在的农业区居民80名为对照组,通过分析电子垃圾拆解地居民体内重金属暴露水平及其氧化应激水平、尿8-羟基脱氧鸟苷(8-Hydroxy-desoxyguanosine, 8-OHdG)水平和人外周血淋巴细胞双微核率,以反映电子垃圾污染环境中重金属污染的人群生物学效应。
本文由两部分组成:
第一部分:电子垃圾拆解地居民体内重金属水平与氧化应激指标的研究
用石墨炉原子吸收法测定全血中铅,镉,镍,和尿样中铅,镉,镍,铜含量;火焰原子吸收法测定血清铜含量。用谷胱甘肽-S转移酶(glutathione S-transferases, GST)、谷胱甘肽(glutathione, GSH)、超氧化物歧化酶(superoxide dismutase, SOD)试剂盒检测血清GSH,GST,SOD等氧化应激指标。用电化学高效液相色谱法测定尿8-OHdG。结果发现:暴露组人群血铅(115.78μg/L)与尿铜(0.03μg/mgCr)的平均水平高于对照组(87.25μg/L, P<0.01; 0.02μg/mgCr, P<0.05),而血清铜(0.80μg/L)、血镍(7.58μg/L)与尿镉(0.001μg/mgCr)的平均水平则低于对照组(0.88μg/L, P<0.01; 13.55μg/L, P<0.01; 0.002μg/mgCr, P<0.05);暴露组血清GST活性(median=19.52 U/ml)和GSH含量(mean=205.39mg/L)显著高于对照组(mean=14.47U/ml, P<0.01;mean=193.32mg/L, P<0.05),而两组血清SOD活性和尿8-OHdG水平未见显著性差异(P<0.05)。提示电子垃圾拆解地居民有较高的铜暴露,但体内仅有铅的蓄积增加。对照组可能有尚未发现的因素引起了机体的氧化应激反应。
第二部分:电子垃圾拆解地居民淋巴细胞双微核率及其影响因素的研究
用淋巴细胞胞质阻滞双微核试验检测人群外周血淋巴细胞双微核率(micronucleated binucleated cells, MNed BNC)。结果表明:暴露组外周血淋巴细胞中位双微核率为4‰,高于对照组(1‰,P<0.01)。血铅水平与淋巴细胞双微核率之间呈正相关关系(r=0.204, P<0.05)。电子垃圾从业史是双微核率升高的危险因素,即有电子垃圾从业史者的双微核率升高的危险性是对照人群的6.7倍(P<0.01)。这可能是暴露人群接触较高铅导致其体内DNA的损伤。这一推测有待在大样本中证实。
Heavy metals including lead, cadmium, copper and nickel, are widely used in various electronic products. Numerous obsolesced electronic products, so-called electronic-waste can cause serious environment problem. When primary dismantling and recycle methods were used in a few plants, certain pollutants such as PBDE, PHA and heavy metals in e-waste can enter environmental media atmosphere, water body and soil, and threaten human health.
It is well known that, heavy metals (such as lead, cadmium, copper and nickel) exists in the environment and can invade into human body, through many ways, resulting the damages of multiple systems in the organisms. For instance, lead had a stronger toxicity in the nervous system, the hematopoietic system, the digestive system, cardiovascular system and immunologic system. Cadmium is a proved carcinogen. Its adverse effects include damages in not only the kidney function and but also the function of the reproductive system in organisms, when they were exposed to Cadmium. Nickel associates with cancer of the respiratory system. Although copper is an essential element in human body, however, excessive level of Cu can cause disorder in the metabolism of the body.
Recent years, widely concern on environment pollution relating to e-waste has been attracted. However, limited data reported that the adverse effects of pollutants from e-waste on the populations. In the present study, we recruited 58 subjects (as the exposure group) from a decade-long e-waste recycling site in southeast China. Another 80 subjects from an agricultural area that was similar to the exposure site in environment and custom, but without known pollution resources were recruited to be control. To evaluate the biological effects of pollutants from the e-waste on the population, levels of heavy metals, the oxidative stress indicators and the urinary 8-Hydroxy-desoxyguanosine (8-OHdG) were analyzed. In addition, frequencies of the micronucleated binucleated cells (MNed BNC) in the studied subjects were determined as well.
Levels of heavy metals and oxidative stress indicators among the populaiton
levels of the lead, cadmium and nickel in the whole blood samples, and levels lead, cadmium, copper and nickel levels in the urine samples were detected using the graphite furnace atomic absorption spectroscopy method. Serum copper level was determined using the flame atomic absorption spectroscopy method. Levels of glutathione S-transferases (GST) and superoxide dismutase (SOD) and glutathione (GSH) activity were anayzed using the commercial kits. Levels of 8-OHdG were determined by high performance liquid chromatograph-electrochemistry method.
The results showed that in the exposed levels of blood Pb (115.78μg/L) and urinary copper (0.03μg/mgCr) were significantly higher than those of the control (blood Pb: 87.25μg/L, P<0.01; urinary Cu: 0.02μg/mgCr, P<0.05); In exposed levels of blood copper and blodd nickel (0.80μg/L, 7.58μg/L) and urinary cadmium (0.001μg/mgCr) were significantly lower, compared to the control (blood Cu: 0.88μg/L, P<0.01; blood Ni: 13.55μg/L, P<0.01; urinary Cd: 0.002μg/mgCr, P<0.05). Levels of serum GST (median: 19.52 U/ml) and GSH (mean±SD: 205.39±31.21mg/L) in the exposed were significantly higher than those in the control (median: 14.47U/ml, P<0.01; mean±SD: 193.32±37.62mg/L, P<0.05). But no significantly difference were observed between the groups in levels of urinary 8-OHdG and serum SOD (P>0.05).
Our findings suggest that the residents who lived in the E-waste recycling site had higher exposure of Cu but an accumulation of only lead in their body was found. In the control there are some unknown factors may cause oxidative stress reactions. Frequencies of micronucleated binucleated cells in the peripheral lymphocytes and its correlative factors
The frequencies of micronucleated binucleated cells (MNed BNC) in the peripheral lymphocytes among the studies subjects were determined using Cytokinesis-Block Micronucleus assay (CBMN). The results showed that the median frequency of MNed BNC in the exposed is 4‰, which was significantly higher than that (median: 1‰) of the control (P<0.01). A positive correlation between the blood lead level and the frequency of MNed BNC was found (r=0.204, P<0.05). We also found that the history of occupational exposure of dismantling E-waste was a risk factor for the elevated frequency of MNed BNC, because the frequencies of MNed BNC in the workers were 6.7 times that of the control (P<0.01)
The findings indicated that the detected DNA damage in the workers may associate with their exposure of higher level of Pb in their bodies, which need to be validated in the larger populations.
近年,电子垃圾产生的环境问题已引起社会的广泛关注。但是有关电子垃圾污染物暴露人群可能的生物学效应研究的报导却十分有限。本研究选择我国南方某电子垃圾拆解地居民58名为暴露组,地理环境和生活习惯相近且无明显已知污染源存在的农业区居民80名为对照组,通过分析电子垃圾拆解地居民体内重金属暴露水平及其氧化应激水平、尿8-羟基脱氧鸟苷(8-Hydroxy-desoxyguanosine, 8-OHdG)水平和人外周血淋巴细胞双微核率,以反映电子垃圾污染环境中重金属污染的人群生物学效应。
本文由两部分组成:
第一部分:电子垃圾拆解地居民体内重金属水平与氧化应激指标的研究
用石墨炉原子吸收法测定全血中铅,镉,镍,和尿样中铅,镉,镍,铜含量;火焰原子吸收法测定血清铜含量。用谷胱甘肽-S转移酶(glutathione S-transferases, GST)、谷胱甘肽(glutathione, GSH)、超氧化物歧化酶(superoxide dismutase, SOD)试剂盒检测血清GSH,GST,SOD等氧化应激指标。用电化学高效液相色谱法测定尿8-OHdG。结果发现:暴露组人群血铅(115.78μg/L)与尿铜(0.03μg/mgCr)的平均水平高于对照组(87.25μg/L, P<0.01; 0.02μg/mgCr, P<0.05),而血清铜(0.80μg/L)、血镍(7.58μg/L)与尿镉(0.001μg/mgCr)的平均水平则低于对照组(0.88μg/L, P<0.01; 13.55μg/L, P<0.01; 0.002μg/mgCr, P<0.05);暴露组血清GST活性(median=19.52 U/ml)和GSH含量(mean=205.39mg/L)显著高于对照组(mean=14.47U/ml, P<0.01;mean=193.32mg/L, P<0.05),而两组血清SOD活性和尿8-OHdG水平未见显著性差异(P<0.05)。提示电子垃圾拆解地居民有较高的铜暴露,但体内仅有铅的蓄积增加。对照组可能有尚未发现的因素引起了机体的氧化应激反应。
第二部分:电子垃圾拆解地居民淋巴细胞双微核率及其影响因素的研究
用淋巴细胞胞质阻滞双微核试验检测人群外周血淋巴细胞双微核率(micronucleated binucleated cells, MNed BNC)。结果表明:暴露组外周血淋巴细胞中位双微核率为4‰,高于对照组(1‰,P<0.01)。血铅水平与淋巴细胞双微核率之间呈正相关关系(r=0.204, P<0.05)。电子垃圾从业史是双微核率升高的危险因素,即有电子垃圾从业史者的双微核率升高的危险性是对照人群的6.7倍(P<0.01)。这可能是暴露人群接触较高铅导致其体内DNA的损伤。这一推测有待在大样本中证实。
Heavy metals including lead, cadmium, copper and nickel, are widely used in various electronic products. Numerous obsolesced electronic products, so-called electronic-waste can cause serious environment problem. When primary dismantling and recycle methods were used in a few plants, certain pollutants such as PBDE, PHA and heavy metals in e-waste can enter environmental media atmosphere, water body and soil, and threaten human health.
It is well known that, heavy metals (such as lead, cadmium, copper and nickel) exists in the environment and can invade into human body, through many ways, resulting the damages of multiple systems in the organisms. For instance, lead had a stronger toxicity in the nervous system, the hematopoietic system, the digestive system, cardiovascular system and immunologic system. Cadmium is a proved carcinogen. Its adverse effects include damages in not only the kidney function and but also the function of the reproductive system in organisms, when they were exposed to Cadmium. Nickel associates with cancer of the respiratory system. Although copper is an essential element in human body, however, excessive level of Cu can cause disorder in the metabolism of the body.
Recent years, widely concern on environment pollution relating to e-waste has been attracted. However, limited data reported that the adverse effects of pollutants from e-waste on the populations. In the present study, we recruited 58 subjects (as the exposure group) from a decade-long e-waste recycling site in southeast China. Another 80 subjects from an agricultural area that was similar to the exposure site in environment and custom, but without known pollution resources were recruited to be control. To evaluate the biological effects of pollutants from the e-waste on the population, levels of heavy metals, the oxidative stress indicators and the urinary 8-Hydroxy-desoxyguanosine (8-OHdG) were analyzed. In addition, frequencies of the micronucleated binucleated cells (MNed BNC) in the studied subjects were determined as well.
Levels of heavy metals and oxidative stress indicators among the populaiton
levels of the lead, cadmium and nickel in the whole blood samples, and levels lead, cadmium, copper and nickel levels in the urine samples were detected using the graphite furnace atomic absorption spectroscopy method. Serum copper level was determined using the flame atomic absorption spectroscopy method. Levels of glutathione S-transferases (GST) and superoxide dismutase (SOD) and glutathione (GSH) activity were anayzed using the commercial kits. Levels of 8-OHdG were determined by high performance liquid chromatograph-electrochemistry method.
The results showed that in the exposed levels of blood Pb (115.78μg/L) and urinary copper (0.03μg/mgCr) were significantly higher than those of the control (blood Pb: 87.25μg/L, P<0.01; urinary Cu: 0.02μg/mgCr, P<0.05); In exposed levels of blood copper and blodd nickel (0.80μg/L, 7.58μg/L) and urinary cadmium (0.001μg/mgCr) were significantly lower, compared to the control (blood Cu: 0.88μg/L, P<0.01; blood Ni: 13.55μg/L, P<0.01; urinary Cd: 0.002μg/mgCr, P<0.05). Levels of serum GST (median: 19.52 U/ml) and GSH (mean±SD: 205.39±31.21mg/L) in the exposed were significantly higher than those in the control (median: 14.47U/ml, P<0.01; mean±SD: 193.32±37.62mg/L, P<0.05). But no significantly difference were observed between the groups in levels of urinary 8-OHdG and serum SOD (P>0.05).
Our findings suggest that the residents who lived in the E-waste recycling site had higher exposure of Cu but an accumulation of only lead in their body was found. In the control there are some unknown factors may cause oxidative stress reactions. Frequencies of micronucleated binucleated cells in the peripheral lymphocytes and its correlative factors
The frequencies of micronucleated binucleated cells (MNed BNC) in the peripheral lymphocytes among the studies subjects were determined using Cytokinesis-Block Micronucleus assay (CBMN). The results showed that the median frequency of MNed BNC in the exposed is 4‰, which was significantly higher than that (median: 1‰) of the control (P<0.01). A positive correlation between the blood lead level and the frequency of MNed BNC was found (r=0.204, P<0.05). We also found that the history of occupational exposure of dismantling E-waste was a risk factor for the elevated frequency of MNed BNC, because the frequencies of MNed BNC in the workers were 6.7 times that of the control (P<0.01)
The findings indicated that the detected DNA damage in the workers may associate with their exposure of higher level of Pb in their bodies, which need to be validated in the larger populations.
引文
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1.王咏梅.自由基与谷胱甘肽过氧化物酶.解放军药学学报, 2005, 21(5): 369-371.
2. FU WLu, LH XU, YY ZHANG, et al., Regulatory effect of reactive oxygen species on apoptosis induced by chemicals. Chinese Journal of Pharmacology and Toxicology, 2002, 16(6): 464-470.
3.梁建成,汪春红,张妍.醋酸铅染毒小鼠DNA损伤及体内抗氧化酶变化.中国公共卫生, 2006, 22(4): 457-458.
4.周蔚,王世鑫,王俊虹.铅对染毒大鼠血清超氧化物歧化酶活性和丙二醛含量的变化.中国职业医学, 2002, 29(2): 19-21.
5. Ye XB, H Fu, JL Zhu, et al., A study on oxidative stress in lead-exposed workers. J Toxicol Environ Health A, 1999, 57(3): 161-172.
6.连灵君,吴晨,徐进.铅染毒导致小鼠DNA损伤与氧化损伤.环境科学学报, 2006, 26(1): 137-141.
7.吴萍,中东晓,赵冰樵.铅对大鼠脑组织脂质过氧化及自由基作用的研究.铁道劳动安全卫生与环保, 1998, 25(2): 91-93.
8.徐进,徐立红,郑一凡.铅暴露引起的小鼠肝脏抗氧化系统损伤.环境科学学报, 2004, 24(6): 1142-1144.
9. Verschaeve L, M Driesen, M Kirsch-Volders, et al., Chromosome distribution studies after inorganic lead exposure. Hum Genet, 1979, 49(2): 147-158.
10.刘晓梅,石龙,金明华.铅和镉对雄性小鼠生殖细胞DNA损伤的研究.中国公共卫生, 2004, 20(3): 311-312.
11.叶细标,傅华,朱靳良.职业接铅工人外周血细胞DNA损伤检测的彗星试验.中华劳动卫生职业病杂志, 2000, 18(1): 51-53.
12.魏肖莹.铅中毒细胞遗传学效应.广东微量元素科学, 1998, 5(4): 54-57.
13. Latinwo LM, VL Badisa, CO Ikediobi, et al., Effect of cadmium-induced oxidative stress on antioxidative enzymes in mitochondria and cytoplasm of CRL-1439 rat liver cells. Int J Mol Med, 2006, 18(3): 477-481.
14.凌艺辉,宾晓农,林丽白.金属镉作业人群的脂质过氧化与抗氧化能力的观察.实用预防医学, 2005, 12(6): 1274-1275.
15. Bertin G and D Averbeck, Cadmium: cellular effects, modifications of biomolecules, modulation of DNA repair and genotoxic consequences (a review). Biochimie, 2006, 88(11): 1549-1559.
16. Waisberg M, P Joseph, B Hale, et al., Molecular and cellular mechanisms of cadmium carcinogenesis. Toxicology, 2003, 192(2-3): 95-117.
17. Emmanouil C, TM Sheehan, and JK Chipman, Macromolecule oxidation and DNA repair in mussel (Mytilus edulis L.) gill following exposure to Cd and Cr(VI). Aquat Toxicol, 2007, 82(1): 27-35.
18.原福胜,马亚萍,赵五红.大气颗粒物对人双核淋巴细胞微核率的影响.环境与健康杂志, 2005, 44(4): 227-228.
19. Palus J, K Rydzynski, E Dziubaltowska, et al., Genotoxic effects of occupational exposure to lead and cadmium. Mutat Res, 2003, 540(1): 19-28.
20. Wegner R, K Radon, R Heinrich-Ramm, et al., Biomonitoring results and cytogenetic markers among harbour workers with potential exposure to river silt aerosols. Occup Environ Med, 2004, 61(3): 247-253.
21. Huff J, RM Lunn, MP Waalkes, et al., Cadmium-induced cancers in animals and in humans. Int J Occup Environ Health, 2007, 13(2): 202-212.
22.孙应彪,陈建华,刘一亚.硫酸镍致大鼠睾丸细胞线粒体及微粒体损伤.中国公共卫生, 2007, 23(4): 503-504.
23. Doreswamy K, B Shrilatha, T Rajeshkumar, et al., Nickel-induced oxidative stress in testis of mice: evidence of DNA damage and genotoxic effects. J Androl, 2004. 25(6): 996-1003.
24.孙应彪,王俊岭,宋媛朝.镍染毒对小鼠脾脏的脂质过氧化损伤.中国公共卫生, 2005, 21(2): 187-188.
25.龚诒芬,尹玉麟,朱茂祥.补硒对镍作业人员脂质过氧化损伤和细胞免疫功能变化的保护研究.卫生研究, 1994, 23(6): 324-327.
26.张晓宇,张敬,张军.镍致癌的分子机制.国外医学卫生学分册, 2005, 32(6): 365-370.
27. Hartwig A, M Asmuss, I Ehleben, et al., Interference by toxic metal ions with DNA repair processes and cell cycle control: molecular mechanisms. Environ Health Perspect, 2002, 110 (5): 797-799.
28.蔡颖,庄志雄,卢次勇.氯化镍在体内诱导大鼠DNA-蛋白质交联.中国药理学与毒理学杂志, 2002, 16(5): 387-390.
29.蔡颖,庄志雄.镍和镉对人外周血淋巴细胞的DNA损伤作用.中国预防医学杂志, 1999, 33(2): 75-77.
30.周春凌,吴永会,焦广宇.镍冶炼烟尘致CHL细胞DNA损伤的彗星试验.工业卫生与职业病, 2005, 31(6): 376-379.
31. Kasprzak KS, FW Sunderman, Jr., and K Salnikow, Nickel carcinogenesis. Mutat Res, 2003, 533(1-2): 67-97.
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5.梁建成,汪春红,张妍.醋酸铅染毒小鼠DNA损伤及体内抗氧化酶变化.中国公共卫生, 2006, 22(4): 457-458.
6.连灵君,吴晨,徐进.铅染毒导致小鼠DNA损伤与氧化损伤.环境科学学报, 2006, 26(1): 137-141.
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16. Theophanides T and J Anastassopoulou, Copper and carcinogenesis. Crit Rev Oncol Hematol, 2002, 42(1): 57-64.
17.周蔚,王世鑫,王俊虹.铅对染毒大鼠血清超氧化物歧化酶活性和丙二醛含量的变化.中国职业医学, 2002, 29(2): 19-21.
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1.王咏梅.自由基与谷胱甘肽过氧化物酶.解放军药学学报, 2005, 21(5): 369-371.
2. FU WLu, LH XU, YY ZHANG, et al., Regulatory effect of reactive oxygen species on apoptosis induced by chemicals. Chinese Journal of Pharmacology and Toxicology, 2002, 16(6): 464-470.
3.梁建成,汪春红,张妍.醋酸铅染毒小鼠DNA损伤及体内抗氧化酶变化.中国公共卫生, 2006, 22(4): 457-458.
4.周蔚,王世鑫,王俊虹.铅对染毒大鼠血清超氧化物歧化酶活性和丙二醛含量的变化.中国职业医学, 2002, 29(2): 19-21.
5. Ye XB, H Fu, JL Zhu, et al., A study on oxidative stress in lead-exposed workers. J Toxicol Environ Health A, 1999, 57(3): 161-172.
6.连灵君,吴晨,徐进.铅染毒导致小鼠DNA损伤与氧化损伤.环境科学学报, 2006, 26(1): 137-141.
7.吴萍,中东晓,赵冰樵.铅对大鼠脑组织脂质过氧化及自由基作用的研究.铁道劳动安全卫生与环保, 1998, 25(2): 91-93.
8.徐进,徐立红,郑一凡.铅暴露引起的小鼠肝脏抗氧化系统损伤.环境科学学报, 2004, 24(6): 1142-1144.
9. Verschaeve L, M Driesen, M Kirsch-Volders, et al., Chromosome distribution studies after inorganic lead exposure. Hum Genet, 1979, 49(2): 147-158.
10.刘晓梅,石龙,金明华.铅和镉对雄性小鼠生殖细胞DNA损伤的研究.中国公共卫生, 2004, 20(3): 311-312.
11.叶细标,傅华,朱靳良.职业接铅工人外周血细胞DNA损伤检测的彗星试验.中华劳动卫生职业病杂志, 2000, 18(1): 51-53.
12.魏肖莹.铅中毒细胞遗传学效应.广东微量元素科学, 1998, 5(4): 54-57.
13. Latinwo LM, VL Badisa, CO Ikediobi, et al., Effect of cadmium-induced oxidative stress on antioxidative enzymes in mitochondria and cytoplasm of CRL-1439 rat liver cells. Int J Mol Med, 2006, 18(3): 477-481.
14.凌艺辉,宾晓农,林丽白.金属镉作业人群的脂质过氧化与抗氧化能力的观察.实用预防医学, 2005, 12(6): 1274-1275.
15. Bertin G and D Averbeck, Cadmium: cellular effects, modifications of biomolecules, modulation of DNA repair and genotoxic consequences (a review). Biochimie, 2006, 88(11): 1549-1559.
16. Waisberg M, P Joseph, B Hale, et al., Molecular and cellular mechanisms of cadmium carcinogenesis. Toxicology, 2003, 192(2-3): 95-117.
17. Emmanouil C, TM Sheehan, and JK Chipman, Macromolecule oxidation and DNA repair in mussel (Mytilus edulis L.) gill following exposure to Cd and Cr(VI). Aquat Toxicol, 2007, 82(1): 27-35.
18.原福胜,马亚萍,赵五红.大气颗粒物对人双核淋巴细胞微核率的影响.环境与健康杂志, 2005, 44(4): 227-228.
19. Palus J, K Rydzynski, E Dziubaltowska, et al., Genotoxic effects of occupational exposure to lead and cadmium. Mutat Res, 2003, 540(1): 19-28.
20. Wegner R, K Radon, R Heinrich-Ramm, et al., Biomonitoring results and cytogenetic markers among harbour workers with potential exposure to river silt aerosols. Occup Environ Med, 2004, 61(3): 247-253.
21. Huff J, RM Lunn, MP Waalkes, et al., Cadmium-induced cancers in animals and in humans. Int J Occup Environ Health, 2007, 13(2): 202-212.
22.孙应彪,陈建华,刘一亚.硫酸镍致大鼠睾丸细胞线粒体及微粒体损伤.中国公共卫生, 2007, 23(4): 503-504.
23. Doreswamy K, B Shrilatha, T Rajeshkumar, et al., Nickel-induced oxidative stress in testis of mice: evidence of DNA damage and genotoxic effects. J Androl, 2004. 25(6): 996-1003.
24.孙应彪,王俊岭,宋媛朝.镍染毒对小鼠脾脏的脂质过氧化损伤.中国公共卫生, 2005, 21(2): 187-188.
25.龚诒芬,尹玉麟,朱茂祥.补硒对镍作业人员脂质过氧化损伤和细胞免疫功能变化的保护研究.卫生研究, 1994, 23(6): 324-327.
26.张晓宇,张敬,张军.镍致癌的分子机制.国外医学卫生学分册, 2005, 32(6): 365-370.
27. Hartwig A, M Asmuss, I Ehleben, et al., Interference by toxic metal ions with DNA repair processes and cell cycle control: molecular mechanisms. Environ Health Perspect, 2002, 110 (5): 797-799.
28.蔡颖,庄志雄,卢次勇.氯化镍在体内诱导大鼠DNA-蛋白质交联.中国药理学与毒理学杂志, 2002, 16(5): 387-390.
29.蔡颖,庄志雄.镍和镉对人外周血淋巴细胞的DNA损伤作用.中国预防医学杂志, 1999, 33(2): 75-77.
30.周春凌,吴永会,焦广宇.镍冶炼烟尘致CHL细胞DNA损伤的彗星试验.工业卫生与职业病, 2005, 31(6): 376-379.
31. Kasprzak KS, FW Sunderman, Jr., and K Salnikow, Nickel carcinogenesis. Mutat Res, 2003, 533(1-2): 67-97.
32.陈瑗,周玫.自由基医学.北京:人民军医出版杜, 1991: 211-215.
33.韦安阳,周春兰.微量元素铜、铁、锰、锗与自由基.广东微量元景科学, 2001, 8(6): 15-16.
34.李筱青,李富军,孙贵范.铜冶炼作业工人职业危害调查. Chinese J Ind Med, 1998, 11(3): 184.
35. Theophanides T, J Anastassopoulou. Copper and carcinogenesis. Crit Rev Oncol Hematol, 2002. 42(1): 57-64.
36.刘璐,严玉仙.铜和致癌作用.国外医学医学地理分册, 2004, 25(1): 29-33.
37. Zheng LF, F Dai, B Zhou, et al., Prooxidant activity of hydroxycinnamic acids on DNA damage in the presence of Cu(II) ions: mechanism and structure-activity relationship. Food Chem Toxicol, 2008, 46(1): 149-156.